4-1 Searching for Electrical Activity in the Nervous System

Electrical stimulation studies dating as far back as the eighteenth century show that stimulating a nerve with electrical current induces a muscle contraction. In more recent recording studies, the brain’s electrical current, measured using an oscilloscope, shows that electrical activity in the nervous system is continuous.

In the twentieth century, researchers used giant axons of the squid to measure the electrical activity of a single neuron. Using microelectrodes that they could place on or in the cell, they recorded small, rapid electrical changes with an oscilloscope. Today, digital oscilloscopes and computers record these measurements.

A neuron’s electrical activity is generated by ions flowing across the cell membrane. Ions flow both down a concentration gradient (from an area of relatively high concentration to an area of lower concentration) and down a voltage gradient (from an area of relatively high voltage to an area of lower voltage). The opening, closing, and pumping of ion channels in neural cell membranes also affect ion distribution.

4-2 Electrical Activity of a Membrane

Unequal ion distribution on a cell membrane’s two sides generates the neuron’s resting potential. At rest, the intracellular membrane registers about –70 mV relative to the extracellular side. Negatively charged protein anions are too large to leave the neuron, and the cell membrane actively pumps out positively charged sodium ions. Unequal distributions of potassium cations and chloride anions contribute to the resting potential as well.

Graded potentials, short-lived small increases or decreases in transmembrane voltage, result when the neuron is stimulated. Voltage changes affect the membrane’s ion channels and in turn change the cross-membrane ion distribution. An increase in transmembrane voltage causes hyperpolarization; a decrease causes depolarization.

An action potential is a brief but large change in axon membrane polarity triggered when the transmembrane voltage drops to a threshold level of about –50 mV. During an action potential, transmembrane voltage suddenly reverses—the intracellular side becomes positive relative to the extracellular side—and abruptly reverses again. Gradually, the resting potential is restored. These membrane changes result from voltage-sensitive channels—sodium and potassium channels sensitive to the membrane’s voltage.

When an action potential is triggered at the initial segment, it can propagate along the axon as a nerve impulse. Nerve impulses travel more rapidly on myelinated axons because of saltatory conduction: the action potentials leap between the nodes separating the glial cells that form the axon’s myelin sheath.

4-3 How Neurons Integrate Information

Inputs to neurons from other cells can produce both excitatory postsynaptic potentials and inhibitory postsynaptic potentials. The membrane sums their voltages both temporally and spatially to integrate the incoming information. If the summed EPSPs and IPSPs move the membrane voltage at the initial segment to threshold, the axon generates an action potential.

The neuron is a versatile kind of cell. Some species’ ion channels respond to light rather than to voltage changes, an attribute that genetic engineers are exploiting. Most of our neurons do not initiate action potentials on dendrites, because the cell body membrane does not contain voltage-sensitive channels. But some voltage-sensitive channels on dendrites do enable action potentials. Back propagation, the reverse movement of an action potential from the initial segment into the dendritic field of a neuron, may play a role in plastic changes that underlie learning.

4-4 Into the Nervous System and Back Out

Sensory receptor cells convert sensory energy to graded potentials. These changes, in turn, alter transmembrane voltage to trigger an action potential and propagate a nerve impulse that transmits sensory information to relevant parts of the nervous system.

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Ion channels come into play to activate muscles as well, because the chemical transmitter acetylcholine, released at the axon terminal of a motor neuron, activates channels on the end plate of a muscle cell membrane. The subsequent ion flow depolarizes the muscle cell membrane to the threshold for its action potential. In turn, this depolarization activates voltage-sensitive channels, producing an action potential on the muscle fiber, hence the muscle contractions that enable movement. In myasthenia gravis, antibodies to the acetylcholine receptor prevent muscle depolarization, which is the basis of weakness and fatigue.